EXPERIMENTAL STUDY FOR REDUCTION OF ISCHEMIA-REPERFUSION INJURY TO SKIN FLAP MODEL BY MONOCLONAL ANTIBODY TO ADHESION MOLECULE.
Project/Area Number |
15591901
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Plastic surgery
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Research Institution | SHOWA UNIVERSITY |
Principal Investigator |
TOSA Yasuyoshi Showa University, Department of Plastic Surgery, Assistant Professor, 医学部, 講師 (60296986)
|
Co-Investigator(Kenkyū-buntansha) |
SATOH Kaneshige Showa University, Department of Plastic Surgery, Professor, 医学部, 教授 (50138442)
HOSAKA Yoshiaki Showa University, Department of Plastic Surgery, Professor, 医学部, 教授 (40156998)
|
Project Period (FY) |
2003 – 2006
|
Project Status |
Completed (Fiscal Year 2006)
|
Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2006: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2005: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2004: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2003: ¥1,000,000 (Direct Cost: ¥1,000,000)
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Keywords | MONOCLONAL ANTIBODY / ISCHEMIA-REPERFUSION INJURY / SKIN FLAP MODEL / ANTIBODY TO LECAM-1 / ANTIBODY TO ELAM-1 / ANTIBODY TO P-SELECTIN / ANIMAL MODEL / Sprague-Dawley Rat / 虚血再潅流障害 / 抗PSGL-1抗体 / 抗selectin抗体 / 抗LECAM-1抗体 / ELAM-1抗体 / 抗L-selectin抗体 / E-selectin抗体 / 抗CD34抗体 / 動物実験 / セレクチンファミリー |
Research Abstract |
Aim : Ischemia-reperfusion (I-R) injury continues to be a problem for successful free tissue transfer and replantation after prolonged periods of ischemia. It has been shown that leukocytes and vascular endothelial cells release a variety of inflammatory mediators during reperfusion after ischemia. The selectin family, which mediates adhesion of activated leukocytes and vascular endothelium in inflammation at lesion sites, is considered to play an important role in the sequence of inflammatory reactions. The selectin family includes LECAM-1, ELAM-1, and P-selectin, which are expressed in activated vascular endothelium and mediates the special leukocyte rolling phenomenon seen when leukocytes adhere to vascular endothelium. The purpose of this study was to evaluate the blockage of leukocyte-endothelial adhesion by a monoclonal antibody (MAb) to LECAM-1, ELAM-1, and P-selectin in skin flaps to prevent I-R injury in rats. Methods : Male SD rats (225-250gr) were used. A skin flap (45x30mm)
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supplied by the superficial epigastric A&V including the femoral vessels was isolated unilaterally. The femoral vessels were cross-clamped the epigastric vessels for 9 hours of ischemia. Animals in treated group received MAb to LECAM-1, ELAM-1, and P-selectin i.v. 15 minutes prior to reperfusion ; those in the control group received normal saline. Skin flap viability was assessed by tracing the outline of viable and nonviable areas. Data were collected for the following 7 days. These data were corroborated with histological evidence on comparable areas of the flap. Results : Tracing analysis revealed average flap survival area of about 80% in treated group and about 20% in control group (p<0.05). Histopathologically, few inflammatory changes could be observed in treated group, while marked damage was observed in control group. Conclusions : From this study, we concluded that treating skin flaps with Mab to LECAM-1, ELAM-1, and P-selectin were effective for I-R injury after 9 hours of warm ischemia. Less
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Report
(5 results)
Research Products
(7 results)